Muñoz H R, Evans R D, Marsch S C, Foëx P
Nuffield Department of Anaesthetics, Radcliffe Infirmary, Oxford, UK.
Cardiovasc Res. 1995 Dec;30(6):1028-32. doi: 10.1016/s0008-6363(95)00181-6.
Platelet-activating factor might be responsible for the alterations of diastolic function observed in different disease states and these potential effects have not been studied. The effect of incremental concentrations of platelet-activating factor (to a maximum of 200 nM) was therefore examined in isolated perfused rat heart. Platelet-activating factor decreased coronary flow rate and contractility in a dose-dependent manner. Although high-dose platelet-activating factor decreased peak -dP/dt compared to baseline, this was not significant when compared to vehicle-administered control. There were no changes in the time constant of left ventricular relaxation and the chamber stiffness constant. These results do not support a major direct role of platelet-activating factor in diastolic dysfunction.
血小板活化因子可能是不同疾病状态下所观察到的舒张功能改变的原因,而这些潜在影响尚未得到研究。因此,在离体灌流的大鼠心脏中检测了递增浓度(最高达200 nM)的血小板活化因子的作用。血小板活化因子以剂量依赖的方式降低冠状动脉血流量和心肌收缩力。尽管高剂量的血小板活化因子与基线相比降低了峰值-dP/dt,但与给予赋形剂的对照组相比,这一差异并不显著。左心室舒张时间常数和心室僵硬度常数没有变化。这些结果不支持血小板活化因子在舒张功能障碍中起主要直接作用。